New Series of Interactive Cardiology MCQs 3

Explanation: NYHA Class III indicates marked limitation of physical activity. Less than ordinary activity causes fatigue, palpitation, or dyspnea, but the patient is comfortable at rest. Class IV patients have symptoms at rest.

Explanation: The Valsalva maneuver (strain phase) decreases venous return (preload) to the heart. In HOCM, a smaller left ventricular volume worsens the outflow tract obstruction, making the murmur louder.

Explanation: The mitral valve is overwhelmingly the most frequently involved valve in rheumatic heart disease, almost always presenting later in life as mitral stenosis.

Explanation: Xanthopsia (seeing yellow-green halos) is a classic neurological manifestation of digoxin toxicity, alongside nausea, vomiting, and characteristic arrhythmias.

Explanation: Stanford Type A dissections involve the ascending aorta and carry a very high risk of rupture or tamponade, requiring emergent open surgical repair. Type B dissections (descending only) can often be managed medically.

Explanation: A normal ABI is between 0.91 and 1.30. Values below 0.90 indicate peripheral arterial disease (PAD), while values above 1.30 suggest non-compressible, calcified vessels.

Explanation: While Amiodarone has characteristics of all four classes, it is primarily categorized as a Class III agent, prolonging phase 3 of the cardiac action potential by blocking potassium channels.

Explanation: Coxsackievirus B (an enterovirus) has historically been recognized as the most common viral cause of acute myocarditis, though parvovirus B19 and HHV-6 are also highly prevalent in recent molecular studies.

Explanation: The major criteria (JNES) include Joint involvement (polyarthritis), (Myocarditis/Carditis), Nodules (subcutaneous), Erythema marginatum, and Sydenham chorea. The others listed are minor criteria.

Explanation: Calcium channel blockers (like diltiazem or amlodipine) promote vasodilation and prevent coronary artery spasm. Beta-blockers (especially non-selective ones) are generally avoided as they can exacerbate vasospasm by leaving alpha-receptors unopposed.

Explanation: Dressler syndrome is a delayed, immune-mediated pericarditis that develops 2 to 10 weeks after a myocardial infarction, differentiating it from early peri-infarction pericarditis.

Explanation: This is the classic description of a VSD murmur. The smaller the defect, the louder and harsher the murmur tends to be due to high turbulence.

Explanation: Wenckebach phenomenon exhibits progressive AV node fatigue, seen as a lengthening PR interval on successive beats until the node fails to conduct, resulting in a dropped QRS.

Explanation: While Tetralogy of Fallot is the most common cyanotic defect overall, TGA is the most common cyanotic lesion presenting in the immediate neonatal period (within the first week of life).

Explanation: Patients with Marfan syndrome have cystic medial necrosis of the aorta, making aortic root dilation leading to aneurysms and catastrophic dissection the primary cause of premature death.

Explanation: The classic presentation of severe symptomatic AS is captured by the acronym SAD: Syncope (especially exertional), Angina, and Dyspnea (heart failure).

Explanation: They are Class Ic antiarrhythmics, which strongly block fast sodium channels, significantly slowing phase 0 depolarization. They are contraindicated in patients with structural heart disease.

Explanation: A normal resting LVEF is typically between 55% and 70%. Values below 50% generally indicate impaired systolic function.

Explanation: BNP (and NT-proBNP) is released by the ventricles in response to volume expansion and pressure overload. It is an excellent marker for heart failure exacerbations.

Explanation: Clopidogrel is a thienopyridine prodrug that irreversibly blocks the P2Y12 component of ADP receptors on the platelet surface, preventing platelet aggregation.

Explanation: The deposition of amyloid proteins between myocardial fibers creates an echogenic, granular “sparkling” or speckled texture classic for restrictive cardiomyopathy due to amyloidosis.

Explanation: Statins are competitive inhibitors of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol biosynthesis. This leads to upregulation of LDL receptors and increased clearance of LDL from the blood.

Explanation: Beta-blockers (like metoprolol) or non-dihydropyridine calcium channel blockers (like diltiazem) are first-line for rate control. Digoxin is a second-line option, and rhythm control agents (Amiodarone, Flecainide) are not used for pure rate control.

Explanation: The Fick principle states that blood flow to an organ (Cardiac Output) can be calculated using a marker substance (usually oxygen). CO = Oxygen consumption / (Arterial O2 content – Venous O2 content).

Explanation: In an ASD, the continuous left-to-right shunt delays pulmonic valve closure equally during both inspiration and expiration, causing a fixed, widely split second heart sound.